Current status and strategies of long noncoding RNA research for diabetic cardiomyopathy.
Current status and strategies of long noncoding RNA research for diabetic cardiomyopathy.
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长链非编码RNA治疗糖尿病心肌病的研究现状及策略
DOI：
10.1186/s12872-018-0939-5
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发表时间：
2018-10-20
影响因子：
2.1
通讯作者：
Ge ZD
中科院分区：
文献类型：
--
作者：
Pant T;Dhanasekaran A;Fang J;Bai X;Bosnjak ZJ;Liang M;Ge ZD
长链非编码RNA（longnoncodingRNA，lncRNA）是一类长度超过200个核苷酸的内源性RNA转录物，它在表观遗传学上调节基因的表达，但不具有蛋白质编码潜力。它们正在成为糖尿病和多种心血管疾病的潜在关键调节剂。糖尿病性心肌病（DCM）是指糖尿病引起的心肌结构和功能异常，而不是由缺血或高血压引起的。本文综述了扩张型心肌病lncRNA的研究现状，探讨了扩张型心肌病lncRNA研究面临的挑战和可能的策略。使用PubMed和Google Scholar数据库进行系统检索。还检索了2014年1月至2018年8月期间发生的糖尿病和心血管疾病的主要会议论文集，以识别可能符合条件的未发表研究。DCM的发病机制涉及代谢紊乱引起的氧化应激、心肌炎症、细胞凋亡和自噬。成千上万的lncRNA在DCM中被异常调节。用遗传学方法操纵特异性lncRNA（如H19、转移相关肺腺癌转录物1和心肌梗死相关转录物）的表达可有效调节实验动物中的氧化应激、心肌炎症、细胞凋亡和自噬并改善DCM。关于DCM中单个lncRNA的调节和功能的详细数据是有限的。然而，lncRNA已被认为是DCM的潜在诊断和治疗靶点。心脏中保护性lncRNA的过表达和有害lncRNA的敲低对于定义目的lncRNA在DCM中的作用和功能至关重要，然而，由于lncRNA的长度、短寿命和位置，它们在技术上具有挑战性。基因递送载体可以提供心脏保护性lncRNA的外源性来源以改善DCM，并且CRISPR-Cas9基因组编辑技术可以用于敲低DCM中的特异性lncRNA。总之，目前的数据表明，LncRNA是DCM的重要调节因子，并作为DCM的有希望的诊断和治疗靶点。
Long noncoding RNAs (lncRNAs) are endogenous RNA transcripts longer than 200 nucleotides which regulate epigenetically the expression of genes but do not have protein-coding potential. They are emerging as potential key regulators of diabetes mellitus and a variety of cardiovascular diseases. Diabetic cardiomyopathy (DCM) refers to diabetes mellitus-elicited structural and functional abnormalities of the myocardium, beyond that caused by ischemia or hypertension. The purpose of this review was to summarize current status of lncRNA research for DCM and discuss the challenges and possible strategies of lncRNA research for DCM. A systemic search was performed using PubMed and Google Scholar databases. Major conference proceedings of diabetes mellitus and cardiovascular disease occurring between January, 2014 to August, 2018 were also searched to identify unpublished studies that may be potentially eligible. The pathogenesis of DCM involves elevated oxidative stress, myocardial inflammation, apoptosis, and autophagy due to metabolic disturbances. Thousands of lncRNAs are aberrantly regulated in DCM. Manipulating the expression of specific lncRNAs, such as H19, metastasis-associated lung adenocarcinoma transcript 1, and myocardial infarction-associated transcript, with genetic approaches regulates potently oxidative stress, myocardial inflammation, apoptosis, and autophagy and ameliorates DCM in experimental animals. The detail data regarding the regulation and function of individual lncRNAs in DCM are limited. However, lncRNAs have been considered as potential diagnostic and therapeutic targets for DCM. Overexpression of protective lncRNAs and knockdown of detrimental lncRNAs in the heart are crucial for defining the role and function of lncRNAs of interest in DCM, however, they are technically challenging due to the length, short life, and location of lncRNAs. Gene delivery vectors can provide exogenous sources of cardioprotective lncRNAs to ameliorate DCM, and CRISPR–Cas9 genome editing technology may be used to knockdown specific lncRNAs in DCM. In summary, current data indicate that LncRNAs are a vital regulator of DCM and act as the promising diagnostic and therapeutic targets for DCM.
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10.1161/atvbaha.114.303240
发表时间：
2014-06
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
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作者：
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DOI：
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发表时间：
2016-07
期刊：
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